Sudan Ebola virus can persist in survivors for months

Image Credit: AI Generated

More than half of survivors of the Sudan Ebola virus still suffer serious health problems two years post-infection and the virus can persist in semen and breast milk for months after recovery, according to the first study examining the virus’s long-term effects.

The study, led by researchers at Washington State University, found 57.5% of the survivors of an outbreak in Uganda from 2022–23 reported ongoing and debilitating health issues that interfered with their daily lives. The detection of traces of the virus in semen and breast milk also raised concerns about the potential for sexual and mother-to-child transmission. The findings were recently published in the journal BMC Medicine.

“This is the first time anyone has been able to closely follow Sudan Ebola survivors over the long term, and the results show the virus continues to affect people’s lives well after an outbreak ends,” said lead researcher Kariuki Njenga, a professor in the WSU College of Veterinary Medicine’s Paul G. Allen School for Global Health and senior scientist at WSU Global Health – Kenya. “Just as concerning is the fact we detected the virus in semen and breast milk, which shows there is a risk survivors could pass on Ebola months after recovery.”

How mosquito-borne viruses breach the brain’s defenses

Stem cell-derived blood-brain barrier cells.
Image Credit: Pablo Alvarez/Li Lab 

Mosquito-borne viruses can cause more than fevers and joint pain. In severe cases, they invade the brain, leading to seizures, encephalitis, lasting memory loss and sometimes death. But thanks to a new UCLA study, researchers have uncovered how some of these viruses breach the brain’s defenses — and point toward ways of keeping them out.

The research, published in Cell Reports, focuses on Sindbis virus, a relatively mild pathogen that scientists use as a safe stand-in for more dangerous mosquito-borne viruses such as chikungunya. 

Using a stem cell-based model of the human blood-brain barrier, developed with collaborators from Florida State University, the UCLA team compared two closely related Sindbis strains — one brain-invading and one not — and found that small changes in viral surface proteins called glycoproteins dictate whether the virus can cross.

The team discovered that the invasive strain grips just one or two specific proteins on blood-brain barrier cells, turning those proteins into doorways that let the virus inside. By contrast, the non-invasive strain spreads its efforts across many receptors and is far less successful.

Koala stress linked to disease threat

Many koalas in the study were successfully treated for Chlamydia before being released back into the wild.
Photo Credit: Currumbin Wildlife Hospital

Researchers have revealed a clear relationship between stress and increased disease risk in koalas in South East Queensland and on the New South Wales North Coast.

A study led by Dr Michaela Blyton at The University of Queensland measured and tracked the level of koala retrovirus (KoRV) in groups of captive and wild koalas.

“We wanted to see what happened to their KoRV loads over time and how it related to chlamydial infection and levels of the stress hormones cortisol and corticosterone in their feces,” Dr Blyton said.

“Virus load likely weakens the immune system, so those with a higher KoRV load are more at risk of diseases such as Chlamydia which can cause blindness, infertility and death.

“Poor quality or disappearing habitat may increase stress and the koalas with higher average cortisol levels had higher average KoRV loads.

Influenza A viruses adapt shape in response to environmental pressures

Colorized transmission electron micrograph of influenza A virus particles, colorized red and gold, isolated from a patient sample and then propagated in cell culture. Influenza A can infect both humans and animals, including birds and pigs. More specifically, this image features the H3N2 influenza strain, isolated from a patient in Victoria, Australia, in 1975. Notable for forming both spheric
Image Credit: National Institute of Allergy and Infectious Diseases

Influenza A virus particles strategically adapt their shape—to become either spheres or larger filaments—to favor their ability to infect cells depending on environmental conditions, according to a new study from National Institutes of Health (NIH) scientists. This previously unrecognized response could help explain how influenza A and other viruses persist in populations, evade immune responses, and acquire adaptive mutations, the researchers explain in a new study published in Nature Microbiology.

The study, led by intramural researchers at NIH’s National Institute of Allergy and Infectious Diseases (NIAID), was designed to determine why many influenza A virus particles exist as filaments. The filament shape requires more energy to form than a sphere, they state, and its abundance has been previously unexplained. To find the answer, they developed a way to observe and measure real-time influenza A virus structure during formation.

UQ team finds relative of deadly Hendra virus in the US

A northern short-tailed shrew
Photo Credit: RPN

Researchers at The University of Queensland have identified the first henipavirus in North America. 

Dr Rhys Parry from the School of Chemistry and Molecular Biosciences said Camp Hill virus was confirmed in shrews in the US state of Alabama.

“Henipaviruses have caused serious disease and death in people and animals in other regions,” Dr Parry said

“One of the most dangerous is the Hendra virus, which was first detected in Brisbane, Australia and has a fatality rate of 70 per cent.

“Another example is Nipah virus which has recorded fatality rates between 40 and 75 per cent in outbreaks in South-East Asia, including in Malaysia and Bangladesh.

“The discovery of a henipavirus in North America is highly significant, as it suggests these viruses may be more globally distributed than previously thought.”

Better prediction of epidemics

The curve calculated using a “reproduction matrix” (turquoise) reflects the actual infection rate (black) much more accurately than previous models (yellow and blue).
Graphic Credit: Empa

The reproduction number R is often used as an indicator to predict how quickly an infectious disease will spread. Empa researchers have developed a mathematical model that is just as easy to use but enables more accurate predictions than R. Their model is based on a reproduction matrix that takes into account the heterogeneity of society.

"Your friends have more friends than you do", wrote the US sociologist Scott Feld in 1991. Feld's so-called friendship paradox states that the friends of any given person have more friends on average than the person themselves. This is based on a simple probability calculation: Well-connected people are more likely to appear in other people's social circles. "If you look at any person's circle of friends, it is very likely that this circle contains very well-connected people with an above-average number of friends," explains Empa researcher Ivan Lunati, head of the Computational Engineering laboratory. A similar principle served Lunati and his team as the basis for a new mathematical model that can be used to more accurately predict the development of case numbers during an epidemic.

Study explains why some osteoporosis drugs may protect against Covid-19

Drugs already in-use for other conditions could help in the fight against Covid-19 and its variants
Photo Credit: Courtesy of University of York

Researchers have provided the molecular explanation for why some osteoporosis drugs offer protection against Covid-19.

Drugs already in-use for other conditions could help in the fight against Covid-19 and its variants

The study, by researchers at the University of York, builds on work conducted by Harvard Medical School that compared more than 450,000 users of a class of drugs, called bisphosphonates, with non-users during the months leading up to the pandemic in 2020. 

The Harvard study showed that those who used drugs, such as alendronate and zoledronate, had lower odds of testing for SARS-CoV-2 infection, Covid-19 diagnosis and Covid-19-related hospitalization, but the study didn’t explain why this was the case.

NIH-funded study finds cases of ME/CFS increase following SARS-CoV-2

Photo Credit: Bruno Aguirre

New findings from the National Institutes of Health’s (NIH) Researching COVID to Enhance Recovery (RECOVER) Initiative suggest that infection with SARS-CoV-2, the virus that causes COVID-19, may be associated with an increase in the number of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) cases. According to the results, 4.5% post-COVID-19 participants met ME/CFS diagnostic criteria, compared to 0.6% participants that had not been infected by SARS-CoV-2 virus.  RECOVER is NIH’s national program to understand, diagnose, prevent, and treat Long COVID.

The research team, led by Suzanne D. Vernon, Ph.D., from the Bateman Horne Center in Salt Lake City, examined adults participating in the RECOVER adult cohort study to see how many met the IOM clinical diagnostic criteria for ME/CFS at least six months after their infection. Included in the analysis were 11,785 participants who had been infected by SARS-CoV-2 and 1,439 participants who had not been infected by the virus. Findings appear in the Journal of General Internal Medicine.

Discovery of how COVID-19 virus replicates opens door to new antiviral therapies

A new study, looking at the replication stage of the SARS-CoV-2 virus that causes COVID-19, discovered important mechanisms in its replication that could be the foundation for new antiviral therapies.
Image Credit: Gerd Altmann

The study, which sets out to investigate how the SARS-CoV-2 virus replicates once it enters the cells, has made surprising discoveries that could be the foundation for future antiviral therapies. It also has important theoretical implications as the replication of the SARS-CoV-2 virus has, so far, received less attention from researchers.

The viral life cycle can be broken down into two main stages: the first stage is where the virus enters the cell. The second stage is replication where the virus uses the molecular machinery of the cell it has infected to replicate itself by building its parts, assembling them into new viruses that can then exit to infect other cells.

The majority of research into SARS-CoV-2 – the causative agent of COVID-19 – has focused on the Spike protein that allows viral entry. This has led to a lack of understanding of how the virus replicates once it has entered the cell.

A new paper led by Dr Jeremy Carlton in collaboration with Dr David Bauer at the Francis Crick Institute, focuses on how the Envelope protein of SARS-CoV-2 controls late stages of viral replication.

Discovery could end global amphibian pandemic

Panamanian golden frog
Photo Credit: Brian Gratwicke/U.S. Fish & Wildlife Service

A fungus devastating frogs and toads on nearly every continent may have an Achilles heel. Scientists have discovered a virus that infects the fungus, and that could be engineered to save the amphibians.

The fungus, Batrachochytrium dendrobatidis or Bd, ravages the skin of frogs and toads, and eventually causes heart failure. To date it has contributed to the decline of over 500 amphibian species, and 90 possible extinctions including yellow-legged mountain frogs in the Sierras and the Panamanian golden frog. 

A new paper in the journal Current Biology documents the discovery of a virus that infects Bd, and which could be engineered to control the fungal disease.

The UC Riverside researchers who found the virus are excited about the implications of their discovery. In addition to helping them learn about how fungal pathogens rise and spread, it offers the hope of ending what they call a global amphibian pandemic. 

“Frogs control bad insects, crop pests, and mosquitoes. If their populations all over the world collapse, it could be devastating,” said UCR microbiology doctoral student and paper author Mark Yacoub. 

“They’re also the canary in the coal mine of climate change. As temperatures get warmer, UV light gets stronger, and water quality gets worse, frogs respond to that. If they get wiped out, we lose an important environmental signal,” Yacoub said. 

New Method Developed to Isolate HIV Particles

The image shows PNF-coated magnetic microbeads that bind HIV particles to their surface.
Image Credit: Torsten John

Researchers at Leipzig University and Ulm University have developed a new method to isolate HIV from samples more easily, potentially making it easier to detect infection with the virus. They focus on peptide nanofibrils (PNFs) on magnetic microparticles, a promising tool and hybrid material for targeted binding and separation of viral particles. They have published their new findings in the journal Advanced Functional Materials.

“The presented method makes it possible to efficiently capture, isolate and concentrate virus particles, which may improve the sensitivity of existing diagnostic tools and analytical tests,” says Professor Bernd Abel of the Institute of Technical Chemistry at Leipzig University. The nanofibrils used – small, needle-like structures – are based on the EF-C peptide, which was first described in 2013 by Professor Jan Münch from Ulm University and Ulm University Medical Center. EF-C is a peptide consisting of twelve amino acids that forms nanoscale fibrils almost instantaneously when dissolved in polar solvents. These can also be applied to magnetic particles. “Using the EF-C peptide as an example, our work shows how peptide fibrils on magnetic particles can have a completely new functionality – the more or less selective binding of viruses. Originally, fibrils of this kind were more likely to be associated with neurodegenerative diseases,” adds Dr Torsten John, co-first author of the study and former doctoral researcher under Professor Abel at Leipzig University. He is now a junior researcher at the Max Planck Institute for Polymer Research in Mainz, Germany.

Researchers a step closer to a cure for HIV

HIV, the AIDS virus (yellow), infecting a human cell
Image Credit: National Cancer Institute

A new study involving University of Bristol researchers has shown a virus-like particle (HLP) can effectively 'shock and kill' the latent HIV reservoir.

By 2030, the World Health Organization (WHO), the Global Fund and UNAIDS are hoping to end the human immunodeficiency virus (HIV) and AIDS epidemic. An international team of researchers led by Professor Eric Arts from the Schulich School of Medicine & Dentistry, Canada, and Dr Jamie Mann, Senior Lecturer at the University of Bristol, has brought us another step closer to meeting this goal, by finding an effective and affordable targeted treatment strategy for an HIV cure. 

In a first, the study published in Emerging Microbes and Infections demonstrated the team's patented therapeutic candidate. The HIV-virus-like-particle (HLP), is 100 times more effective than other candidate HIV cure therapeutics for people living with chronic HIV on combined antiretroviral therapy (cART). If successful in clinical trials, HLP could be used by millions of people living around the world to free them of HIV. This study was done using blood samples from people living with chronic HIV. 

HLPs are dead HIV particles hosting a comprehensive set of HIV proteins that increase immune responses without infecting a person. When compared with other potential cure approaches, HLP is an affordable biotherapeutic and can be administered by intramuscular injection – similar to the seasonal flu vaccine. 

Research offers hope for preventing post-COVID ‘brain fog’ by targeting brain’s blood vessels

Blood vessel endothelial cells (green) and basement membrane (red) in the brain.
Image Credit: Sarah Lutz

Among the many confounding symptoms in patients recovering from a COVID-19 infection are memory loss and difficulty learning. Yet little is known about the mechanisms of cognitive impairments like these, commonly called brain fog. 

In a new study, researchers at the University of Illinois Chicago have identified a mechanism that causes neurological problems in mice infected with SARS-CoV-2, the virus behind COVID-19. The researchers also found a treatment that helped prevent these changes. Sarah Lutz, assistant professor of anatomy and cell biology in the College of Medicine, led the research, which was published in the journal Brain.

The team focused on the blood-brain barrier, which plays a role in other neurological diseases, such as multiple sclerosis. Normally, this barrier protects the brain from potentially harmful cells or molecules circulating in the bloodstream. But the infected mice, researchers found, had leaky blood-brain barrier vessels and impaired memory or learning.

To understand why, the researchers looked at blood vessels from the brains of infected mice to see which genes were most altered. They found a significant decrease in a signaling pathway called Wnt/beta-catenin, which helps maintain the health of the blood-brain barrier and protects the brain from damage.

Long COVID linked to persistently high levels of inflammatory protein: a potential biomarker and target for treatments

"We hope that this could help to pave the way to develop therapies and give some patients a firm diagnosis," -Benjamin Krishna
Photo Credit: Annie Spratt

SARS-CoV-2 triggers the production of the antiviral protein IFN-γ, which is associated with fatigue, muscle ache and depression. New research shows that in Long COVID patients, IFN-y production persists until symptoms improve, highlighting a potential biomarker and a target for therapies.

A University of Cambridge-led study identifies the protein interferon gamma (IFN-γ) as a potential biomarker for Long COVID fatigue and highlights an immunological mechanism underlying the disease, which could pave the way for the development of much needed therapies, and provide a head start in the event of a future coronavirus pandemic. 

The study, published today in Science Advances, followed a group of patients with Long COVID fatigue for over 2.5 years, to understand why some recovered and others did not. 

Long COVID continues to affect millions of people globally and is placing a major burden on health services. An estimated 1.9 million people in the UK alone (2.9% of the population) were experiencing self-reported Long COVID as of March 2023, according to the ONS. Fatigue remains by far the most common and debilitating symptom and patients are still waiting for an effective treatment.

Targeting inflammation to tackle long covid

Illustration Credit: Gerd Altmann

Overactivation of the immune system leading to circulation of inflammatory proteins around the body contributes to the development of long covid, and could be targeted to provide treatments for patients, finds new research.

Cardiff University research has uncovered biological markers that could be targeted by repurposing medication to treat long covid.

The research conducted extensive analysis of plasma samples obtained from a large cohort of healthy post-covid individuals and non-hospitalized patients with long covid. They found that the complement system – a system that plays a crucial part of the immune system, consisting of a group of proteins that work together to enhance the function of antibodies and immune cells – was commonly overactivated in those with long covid.

“The covid-19 pandemic has left a global legacy of ill health, with long covid estimated to affect up to 1.9 million people in the UK. Long covid can last for months or years after the triggering infection and is associated with diverse symptoms including brain fog, chest pain, breathlessness, fatigue, and sensory problems. The causes of this disease remain largely unknown, emerging evidence suggests an important role for chronic inflammation."
Professor Paul Morgan 'Professor of complement biology, Division of Infection and Immunity

New COVID vaccine induces good antibody response to mutated viral variants

Photo Credit: CDC

Researchers at Karolinska Institutet and Danderyd Hospital have followed recipients of the new updated COVID-19 vaccine and analyzed the antibody response to different SARS-CoV-2 variants. The results show a surprisingly strong response to the now dominant and highly mutated Omicron variants.

The ongoing COMMUNITY study, which was launched in the spring of 2020 with the regular testing of 2,149 members of the Danderyd Hospital staff, has recently published the results of this autumn’s leg of the study. Twenty-four participants were recorded in this study, the majority of whom were over 64 and had received four or five previous vaccine doses. The article has been peer-reviewed and accepted for publication in the scientific journal The Lancet Infectious Diseases, and is accessible prior to publication on the preprint server, bioRxiv.

Deadly chicken disease: ancient DNA reveals evolution of virulence

With the increase in poultry farming, Marek's disease virus evolved
Photo Credit: Heidi-Ann Fourkiller

Using genetic analyses, an international team led by LMU paleogeneticist Laurent Frantz has revealed the evolutionary history of the pathogen of a fatal disease in chickens.

A notifiable animal disease in Germany, Marek’s disease is caused by the globally distributed Marek’s disease virus (MDV). Over the past century, the virus, which causes tumors in chickens and has a high mortality rate, has become increasingly aggressive. Combating the disease costs the poultry industry over a billion dollars every year. With the help of ancient DNA, an international team of scientists led by LMU paleogenomicist Professor Laurent Frantz and Professor Greger Larson and Professor Adrian Smith from the University of Oxford has now decoded the evolution of MDV and shed light on what is behind the growing virulence.

The international team from the fields of paleogenetics, archeology, and biology isolated viral genomes from chicken bones up to 1,000 years old from 140 archeological sites in Europe and the Near East. “Our data shows that the virus was already widely distributed at least 1,000 years before the first description of the disease in 1907,” says Frantz. When the disease was first described, it was said to produce only mild symptoms in older chickens. With the dramatic increase in poultry farming in the 1950s and 1960s, the virus evolved and has become increasingly virulent despite the development of several vaccines.

How the Immune System Fights to Keep Herpes at Bay

These microscope images show how interferon in the nucleus raises levels of the protective protein IFI16 (stained green) from low background levels (left) to the higher levels needed to resist herpes infection (right).
Image Credit: HMS MicRoN core imaging facility/Nicolas Romero Rata

Herpes simplex virus (HSV) is extremely common, affecting nearly two-thirds of the world’s population, according to the World Health Organization.

Once inside the body, HSV establishes a latent infection that periodically awakens, causing painful blisters on the skin, typically around the nose and mouth. While a mere nuisance for most people, HSV can also lead to dangerous eye infections and brain inflammation in some people and cause life-threatening infections in newborns.

Researchers have long known that the virus and the host immune system are in a perpetual competition, but why does this battle reach a stasis in most people while causing serious infections in others?

More important, precisely how does the battle unfold at the level of cells and molecules? This question has continued to bedevil scientists and hamper the quest for treatments that prevent or cure infections.

A recent study by researchers at Harvard Medical School, conducted using lab-engineered cells and published in PNAS, unveils the precise maneuvers used by host and pathogen in the fight for dominance of the cell.

Temperature increase triggers viral infection

Illustration of phage virus injecting its DNA into a cell
Illustration Credit: Alex Evilevitch and Ting Liu

Researchers at Lund University, together with colleagues at the NIST Synchrotron Facility in the USA, have mapped on an atomic level what happens in a virus particle when the temperature is raised.

"When the temperature rises, the virus's genetic material changes its form and density, becoming more fluid-like, which leads to its rapid injection into the cell," says Alex Evilevitch who led the study.

Viruses lack their own metabolism and the ability to replicate independently; they are entirely dependent on a host cell to multiply. Instead, the virus hijacks the internal machinery of the infected cell to produce new virus particles, which are then released and spread to infect other cells.

In most cases, the virus's genetic material, DNA, is enclosed within a protective protein shell called a capsid. A research group at Lund University is working to understand the process by which the virus ejects its genetic material from the capsid and into cells and what causes the virus's DNA to be released.

It all began with a study published in 2014, where the Lund University researchers observed that there seems to be a sudden change in the virus's genetic material when exposed to the infection temperature, around 37 degrees.

Success of Wolbachia-infected mosquitoes in fighting dengue may be underestimated

Alex Perkins, associate professor of biological science
Photo Credit: Courtesy of University of Notre Dame

The fight against dengue fever has a new weapon: a mosquito infected with the bacteria Wolbachia, which prevents the spread of the virus. These mosquitoes have now been deployed in several trials demonstrating their potential in preventing disease transmission.

Now, researchers at the University of Notre Dame have conducted an analysis of the World Mosquito Program’s randomized control trial of Wolbachia-infected mosquitoes in Indonesia, looking at how excluding transmission dynamics impacted the original interpretation of the trial’s results.

“Randomized controlled trials are the gold standard for evaluating the efficacy of any medical or public health intervention. That is very difficult for vector interventions against dengue because incidence of the disease can be somewhat unpredictable and sporadic, requiring very large-scale trials,” said Alex Perkins, associate professor of biological sciences at Notre Dame and senior author on the study.